285 research outputs found

    The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

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    Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury

    University–industry linkages and academic engagements: individual behaviours and firms’ barriers. Introduction to the special section

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    The article introduces the special section on “University–industry linkages and academic engagements: Individual behaviours and firms’ barriers”. We first revisit the latest developments of the literature and policy interest on university–industry research. We then build upon the extant literature and unpack the concept of academic engagement by further exploring the heterogeneity of UI linkages along a set of dimensions and actors involved. These are: (1) Incentives and behaviours of individual academic entrepreneurs; (2) Firms’ barriers to cooperation with public research institutions; (3) Individual behaviours, incentives and organizational bottlenecks in late developing countries. We summarize the individual contributions along these dimensions. There are overlooked individual characteristics that affect the degree of engagement of academics and scholars in cooperating with other organizations, of which gender and the non-academic background of individuals are most crucial. The notion of academic engagement should be enlarged to aspects that go beyond the commercialization or patenting of innovation, but embrace social and economic impact more at large. From the perspective of the firm, barriers to innovation might exert an effect on the likelihood to cooperate with universities and public research institutes, most especially to cope with lack of finance or access to frontier knowledge. We finally propose a research agenda that addresses the challenges ahead

    Empty Urbanism: the bursting of the Spanish housing bubble

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    The depth of the Spanish housing crisis manifests itself in the collapse of construction activity and in the amount of housing and land stocks. The geography of the crisis shows its widespread nature, and the intensity of the previous bubble explains spatial differences. Resulting from this collapse are some problematic areas of 'empty urbanism'. An enormous land bubble, emerging from the peculiar Spanish urban development model, was a key factor in the impacts - caused by the crisis - on the territory and land-use plans. The crisis has demonstrated the unsustainability of this and the urgency of change in the existing land-use plans

    Excessive TV viewing and cardiovascular disease risk factors in adolescents. The AVENA cross-sectional study

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    <p>Abstract</p> <p>Background</p> <p>Excessive television (TV) viewing might play an important role in the development of cardiovascular disease (CVD). The aim of this study was to examine the independent associations between TV viewing and CVD risk factors in adolescents.</p> <p>Methods</p> <p>A sample of 425 adolescents, aged 13- to 18.5-year-old, was included in this study. Body mass index (BMI), waist circumference (WC), glucose, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, apolipoprotein (apo) A-1, apo B-100, and lipoprotein(a) levels were determined. A composite CVD risk score was computed based on age-, sex-, sexual maturation- and race-standardized triglycerides, HDL-cholesterol, LDL-cholesterol and glucose. TV viewing was self-reported.</p> <p>Results</p> <p>Two hundred and twenty-five adolescents (53%) who spent >3 hrs/day watching TV were considered as the "high TV viewing" group. Ninety-nine adolescents (23%) from the total sample were classified as overweight according to International age- and sex-specific BMI values. The high TV viewing group had significantly less favorable values of HDL-cholesterol, glucose, apo A1 and CVD score, independent of age, sex, sexual maturation, race and weight status. There was a significant interaction effect of TV viewing × weight status (P = 0.002) on WC, and the negative influence of TV viewing on WC persisted in the overweight group (P = 0.031) but was attenuated in non-overweight adolescents (P > 0.05).</p> <p>Conclusion</p> <p>Excessive TV viewing seems to be related to an unfavorable CVD risk factors profile in adolescence. Reducing TV viewing in overweight adolescents might be beneficial to decrease abdominal body fat.</p

    Individual Shrink Wrapping of Zucchini Fruit Improves Postharvest Chilling Tolerance Associated with a Reduction in Ethylene Production and Oxidative Stress Metabolites

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    We have studied the effect of individual shrink wrapping (ISW) on the postharvest performance of refrigerated fruit from two zucchini cultivars that differ in their sensitivity to cold storage: Sinatra (more sensitive) and Natura (more tolerant). The fruit was individually shrink wrapped before storing at 4°C for 0, 7 and 14 days. Quality parameters, ethylene and CO2 productions, ethylene gene expression, and oxidative stress metabolites were assessed in shrink wrapped and non-wrapped fruit after conditioning the fruit for 6 hours at 20°C. ISW decreased significantly the postharvest deterioration of chilled zucchini in both cultivars. Weight loss was reduced to less than 1%, pitting symptoms were completely absent in ISW fruit at 7 days, and were less than 25% those of control fruits at 14 days of cold storage, and firmness loss was significantly reduced in the cultivar Sinatra. These enhancements in quality of ISW fruit were associated with a significant reduction in cold-induced ethylene production, in the respiration rate, and in the level of oxidative stress metabolites such as hydrogen peroxide and malonyldialdehyde (MDA). A detailed expression analysis of ethylene biosynthesis, perception and signaling genes demonstrated a downregulation of CpACS1 and CpACO1 genes in response to ISW, two genes that are upregulated by cold storage. However, the expression patterns of six other ethylene biosynthesis genes (CpACS2 to CpACS7) and five ethylene signal transduction pathway genes (CpCTR1, CpETR1, CpERS1, CpEIN3.1 and CpEN3.2), suggest that they do not play a major role in response to cold storage and ISW packaging. In conclusion, ISW zucchini packaging resulted in improved tolerance to chilling concomitantly with a reduction in oxidative stress, respiration rate and ethylene production, as well as in the expression of ethylene biosynthesis genes, but not of those involved in ethylene perception and sensitivity.This work was supported by grants AGL2011-30568-C02/ALI from the Spanish Ministry of Science and Innovation, and AGR1423 from the Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, Spain. Z.M. acknowledges FPU program scholarships from MEC, Spain. S.M. is funded by grant PTA2011-479-I from the Spanish Ministry of Science and Innovation

    Atypical Mg-poor Milky Way Field Stars with Globular Cluster Second-generation-like Chemical Patterns

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    We report the peculiar chemical abundance patterns of 11 atypical Milky Way (MW) field red giant stars observed by the Apache Point Observatory Galactic Evolution Experiment (APOGEE). These atypical giants exhibit strong Al and N enhancements accompanied by C and Mg depletions, strikingly similar to those observed in the so-called second-generation (SG) stars of globular clusters (GCs). Remarkably, we find low Mg abundances ([Mg/Fe] < 0.0) together with strong Al and N overabundances in the majority (5/7) of the metal-rich ([Fe/H] gsim −1.0) sample stars, which is at odds with actual observations of SG stars in Galactic GCs of similar metallicities. This chemical pattern is unique and unprecedented among MW stars, posing urgent questions about its origin. These atypical stars could be former SG stars of dissolved GCs formed with intrinsically lower abundances of Mg and enriched Al (subsequently self-polluted by massive AGB stars) or the result of exotic binary systems. We speculate that the stars Mg-deficiency as well as the orbital properties suggest that they could have an extragalactic origin. This discovery should guide future dedicated spectroscopic searches of atypical stellar chemical patterns in our Galaxy, a fundamental step forward to understanding the Galactic formation and evolution

    S100A14 Stimulates Cell Proliferation and Induces Cell Apoptosis at Different Concentrations via Receptor for Advanced Glycation End Products (RAGE)

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    S100A14 is an EF-hand containing calcium-binding protein of the S100 protein family that exerts its biological effects on different types of cells. However, exact extracellular roles of S100A14 have not been clarified yet. Here we investigated the effects of S100A14 on esophageal squamous cell carcinoma (ESCC) cell lines. Results demonstrated that low doses of extracellular S100A14 stimulate cell proliferation and promote survival in KYSE180 cells through activating ERK1/2 MAPK and NF-κB signaling pathways. Immunoprecipitation assay showed that S100A14 binds to receptor for advanced glycation end products (RAGE) in KYSE180 cells. Inhibition of RAGE signaling by different approaches including siRNA for RAGE, overexpression of a dominant-negative RAGE construct or a RAGE antagonist peptide (AmphP) significantly blocked S100A14-induced effects, suggesting that S100A14 acts via RAGE ligation. Furthermore, mutation of the N-EF hand of S100A14 (E39A, E45A) virtually reduced 10 µg/ml S100A14-induced cell proliferation and ERK1/2 activation. However, high dose (80 µg/ml) of S100A14 causes apoptosis via the mitochondrial pathway with activation of caspase-3, caspase-9, and poly(ADP-ribose) polymerase. High dose S100A14 induces cell apoptosis is partially in a RAGE-dependent manner. This is the first study to demonstrate that S100A14 binds to RAGE and stimulates RAGE-dependent signaling cascades, promoting cell proliferation or triggering cell apoptosis at different doses
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